Wednesday, January 26, 2011

Acute hemorrhagic Leucoencefalita

Acute hemorrhagic Leucoencefalita Leucoencefalita is an inflammation of the white matter of the cerebral hemispheres. Acute hemorrhagic Leucoencefalita is also known as the Hurst disease and is characterized by a severe leucoencefalita shaped, disseminated, of unknown etiology. It is a rare and very serious and evolving finish hiperacut often death. In terms of disease pathology is distinguished by the presence of inflammatory lesions, vascular lesions with necrotic small vessels and hemorrhage. Perivascular lesions manifested by demyelination. Perivenous demyelination and infiltrates of mononuclear and polymorphonuclear inflammatory cells in particular are the most important pathological changes. After vasculitis venules walls become thinner and necroses, small necrotic foci can conflict resulting in large areas of necrosis. White matter of cerebral hemispheres is studded with punctiform hemorrhages and fibrin deposits. These changes pertain to the white matter of the brainstem and spinal cord.
Clinical symptoms pseudotumoral evolves into an epileptic seizure. The clinical picture resembles that of acute disseminated encephalomyelitis in bad shape, but the onset of symptoms and evolution may be more severe. Clinical manifestations are dominated by signs of meningeal irritation (headache, fever, neck stiffness), impaired consciousness, convulsions, muscle weakness, signs of intracranial hypertension and cranial nerves (nerves III and IV). Other manifestations are exacerbated tendon reflexes, Babinski sign present, parkinsonian tremor, focal neurological signs. Some rare cases the disease can pass from acute hemorrhagic leucoencefalita in acute disseminated encephalomyelitis.
Diagnostic Laboratory It will perform a lumbar puncture to collect cerebrospinal fluid. Cytology revealed a sharp Pleocytosis mononuclear up to 3000 cells/mm3. Albuminorahia is also increased and red blood cells are present in variable number. We noticed a major alkaline autoimmune reaction to the protein as in the case of acute encephalomyelitis. ESR is elevated in peripheral blood leucocytes and is present. EEG can be changed, showing signs of outbreak. Brain computed tomography shows the presence of focal lesions. MRI is useful in the spinal lesions and for highlighting areas of demyelination and cerebral edema.
Differential diagnosis will be made with bacterial brain acute viral encephalitis, venous thrombosis, multiple embolic infarctions.
Infaust prognosis is in many cases, can cause severe clinical death within 4-5 days after onset.
Treatment is generally similar to that of acute disseminated encephalomyelitis, the treatment regimen including high dose methylprednisolone and prednisone. A regimen can be given is: slowly administered intravenous methylprednisolone 1000 mg daily for 3 days followed by oral prednisone at a dose of 1 mg / kg / day until day 17 of treatment, then day 18 is given 20 mg / day prednisone, and by day 21 are given 10 mg / day prednisone.

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